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Axonal hyperpolarization in inclusion-body myopathy, paget disease of the bone, and frontotemporal dementia (IBMPFD)
Journal article   Peer reviewed

Axonal hyperpolarization in inclusion-body myopathy, paget disease of the bone, and frontotemporal dementia (IBMPFD)

K.R. Kumar, C. Liang, M. Needham, D. Burke, C.M. Sue and K. Ng
Muscle & Nerve, Vol.44(2), pp.191-196
2011
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Abstract

Introduction: Inclusion-body myopathy, Paget disease of the bone, and frontotemporal dementia (IBMPFD) is an autosomal dominant disorder due to mutations in the valosin-containing protein (VCP) gene. Patients with this disorder may have neuropathic or myopathic features. Methods: Peripheral nerve function and axonal excitability were studied in three members from two families with VCP mutations (p.Arg155Leu and p.Leu198Trp). Results: Patients from the first family had neurogenic patterns on needle electromyography (EMG), whereas those in the second family had myopathic EMG changes. In threshold electrotonus for motor axons, the changes to depolarizing and hyperpolarizing conditioning currents were at or outside control limits in all three patients. Superexcitability was increased, and the relative refractory period was reduced. The strength–duration time constant was normal. In sensory axons of all three patients, there were similar changes in threshold electrotonus, but not in superexcitability. Discussion: These features are best explained by axonal hyperpolarization. The findings provide insight into the pathophysiological mechanisms in these genotypes and, possibly, into all patients with IBMPFD. Muscle Nerve, 2011

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Collaboration types
Domestic collaboration
Citation topics
1 Clinical & Life Sciences
1.79 Molecular & Cell Biology - Physiology
1.79.239 Ion Channelopathies
Web Of Science research areas
Clinical Neurology
Neurosciences
ESI research areas
Neuroscience & Behavior
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